Sprouting of A‐fibre primary afferents into lamina II in two rat models of neuropathic pain

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Abstract
Following peripheral nerve section, injured sensory A‐fibres into lamina II of the dorsal horn and form aberrant functional synapses. Such structural changes may underlie some of the sensory abnormalities observed in nerve‐injured patients, including neuropathic pain. This study compared the ability of intact and injured A‐fibres to sprout in two experimental models of neuropathic pain, where the onset and presence of abnormal behaviours indicative of neuropathic pain have been well described. Rats received either a unilateral chronic constriction injury of the sciatic nerve (CCI) or lesion of the L5 spinal nerve (SNL). The central distribution of the injured and uninjured afferents labelled with choleragenoid conjugated to horseradish peroxidase (B‐HRP) was examined at different postoperative survival times. In both models, the contralateral uninjured side, used for control nerve or ganglion injections, showed labelling of the L3–6 spinal segments in laminae I, III‐V, leaving lamina II unlabelled. In CCI rats, injured sciatic afferents sprouted in lamina II of the L4–5 dorsal horn by 10 days postinjury. In SNL rats, injured L5 afferents sprouted into lamina II of the L4–5 dorsal horn by 24 h postinjury and were robust from 3 to 10 days. In both models, the labelling in lamina II was absent by 4 months. Labelling of the adjacent uninjured saphenous or intact L4 spinal nerve afferents did not reveal A‐fibre sprouting. As the time‐course of sprouting of injured A‐fibres parallels the previously described behaviour interpreted as neuropathic pain in these models, this may be a phenomenon that contributes to sensory abnormalities such as ongoing pain and mechanical hypersensitivity.